A 56-day feeding trial was conducted in a flow-through seawater system to investigate the effects of lysophosphatidylcholine (LPC) on growth performance and lipid metabolism of turbot. Four experimental diets were prepared, differing only in the LPC supplementation, namely, 0 (LPC-0, control), 0.1 (LPC-0.1), 0.25 (LPC-0.25), and 0.5 (LPC-0.5) of dry matter. Each diet was randomly fed to triplicate tanks. LPC-0.1 and LPC-0.25 led to significantly higher weight gain than the control diet, and the highest weight gain was observed in LPC-0.1. Compared to the control group, the LPC-supplemented groups had higher survival and lower hepatosomatic index and viscerosomatic index. LPC-0.25 led to significantly lower contents of crude lipid and ash in whole fish. Dietary LPC supplementation led to a basic decrease in the lipid metabolism-related biochemical parameters in serum but had only very minor influence on the fatty acid composition in the liver and subcutaneous tissue around the fin (STF). High LPC levels upregulated the mRNA expression of BSAL and ApoEα in both the liver and STF. In conclusion, dietary LPC supplementation (0.1-0.25) enhanced the growth, lowered the lipid accumulation in juvenile turbot, and significantly regulated the lipid metabolism. However, it seldom influenced the fatty acid composition.

Two 70-day feeding trials were conducted to reevaluate the necessity of cholesterol supplementation in diets of two important marine fish species, turbot and tiger puffer. Graded levels (0, 0.5, 1.0, 2.0, and 4.0 of dry matter) of cholesterol were added into the basal diet (with 30 fishmeal but no fish oil) to make five experimental diets, which were designated as control, CHO-0.5, CHO-1.0, CHO-2.0, and CHO-4.0, respectively. The dietary cholesterol concentration was measured to be 0.11, 0.65, 1.10, 2.32, and 4.59, respectively. Each group had triplicate tanks, and each tank was stocked with 30 fish. The results showed that compared to the control, dietary cholesterol supplementation had no significant effect on the growth of both turbot and tiger puffer. Nevertheless, excess dietary cholesterol (CHO-2.0 and CHO-4.0) led to significant lower weight gain of tiger puffer compared to CHO-1.0. The feed intake decreased with increasing levels of dietary cholesterol. In general, the cholesterol supplementation decreased the crude lipid content in the liver, whereas 0.5 dietary cholesterol supplementation tended to increase the crude lipid content in the muscle of both species. Dietary cholesterol supplementation significantly regulated the lipid-related biochemical parameters in serum, liver, and muscle, and compared to turbot, tiger puffer lipid compositions had a higher buffering capacity in response to changes in dietary cholesterol level. Dietary cholesterol supplementation increased the 20:4n-6 content in the liver. Dietary cholesterol supplementation significantly downregulated the gene expression of HMG-COAr, upregulated the CYP7A1 expression, and downregulated the expression of lipid absorption and biosynthesis genes, but had no significant effect on gene expression of CPT1 and lipid transport-related genes (ApoA1, ApoA4, ApoB100, and ApoEα) in the liver. In conclusion, under the present experimental condition, dietary cholesterol supplementation had no significant effect on the growth of turbot and tiger puffer. In both species, dietary cholesterol supplementation significantly regulated the lipid accumulation and metabolism.